ECEESPE2025 Rapid Communications Rapid Communications 4: Pituitary, Neuroendocrinology and Puberty Part 1 (6 abstracts)
Melatonin as a possible stimulus to unmask an oxytocin deficient state in hypopituitarism and hypothalamic damage
Queralt Asla Roca 1,2,3 , Maite Garrido Sánchez 4 , Eulàlia Urgell Rull 5 , Sílvia Terzan Molina 5 , Alicia Santos Vives 6,7,8 , Nimmy Varghese 9,10 , Cihan Atila 11,12 , Betina Biagetti 6,13 , Franziska Plessow 14,15 , Mirjam Christ-Crain 11,12 , Anne Eckert 9,10 , Susan M Webb 4,6,7 , Elizabeth A Lawson 14,15 & Anna Aulinas Maso 3,6,8
1Hospital de la Santa Creu i Sant Pau, ENDO-ERN, Department of Endocrinology and Nutrition, Barcelona, Spain; 2Institut de Recerca Sant Pau (IR-SANT PAU), Barcelona, Spain; 3University of Vic-Central University of Catalonia (UVic-UCC), Faculty of Medicine, Vic/Manresa, Catalonia, Spain; 4Institut de Recerca Sant Pau (IR-SANT PAU), Centre d’Investigació del Medicament (CIM), Barcelona, Spain; 5Hospital de la Santa Creu i Sant Pau, Department of Biochemistry, Barcelona, Spain; 6Instituto de Salud Carlos III, Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBER-ER, Unit 747), Majadahonda, Spain; 7Universitat Autònoma de Barcelona, Department of Medicine, Bellaterra, Spain; 8Hospital de la Santa Creu i Sant Pau, IR-SANT PAU, ENDO-ERN, Department of Endocrinology and Nutrition, Barcelona, Spain; 9Universität Basel, Research Cluster Molecular and Cognitive Neurosciences, Basel, Switzerland; 10University Psychiatric Clinics Basel, Neurobiology Lab for Brain Aging and Mental Health, Basel, Switzerland, 11Universitätsspital Basel, Department of Endocrinology, Diabetology and Metabolism, Basel, Switzerland; 12Universität Basel, Department of Clinical Research, Basel, Switzerland; 13Hospital Universitari Vall d’Hebron, ENDO-ERN, Department of Endocrinology and Nutrition, Barcelona, Spain; 14Massachusetts General Hospital, Neuroendocrine Unit, Boston, United States; 15Harvard Medical School, Boston, United States
JOINT591
Introduction: Emerging evidence supports the presence of oxytocin deficiency (OXT-D) in patients with hypopituitarism and hypothalamic damage (HHD). However, the lack of reliable diagnostic tests for OXT-D remains a critical gap. Melatonin might be a candidate for such a test as melatonin receptors are located in the hypothalamus where OXT is synthesized, and melatonin regulates OXT release in animals. This study aimed to examine plasma OXT dynamics in response to oral melatonin in patients with HHD compared to healthy controls (HC) and explore its associations with psychopathology, sexual function, and quality of life (QoL).
Methods: This proof-of-concept study (NCT05319301) included 20 participants with HHD (11 females) and 20 HC (11 females). Melatonin (1.95 mg) was administered sublingually between 8-9 am. Blood samples were collected over 120 minutes. Additionally, participants were asked to complete questionnaires to assess psychopathology, sexual function and QoL. Linear mixed-effects regression model controlled for body mass index (BMI) was used to evaluate the change in OXT over time in HHD compared to HC.
Results: Both groups were comparable in age and gender distribution. The median BMI was higher in the HHD compared to the HC group (30.20 (3.79) vs. 22.91 (7.34) kg/m2, P=0.02). Baseline OXT levels were similar across groups (HHD 56.75±4.13 vs. HC 57.05±3.99 pg/ml, P=0.86). In HC, melatonin significantly increased OXT at T90 vs. T0, whereas no such increase was observed in the HHD group (68.95±4.37 vs. 54.07±4.37 pg/ml, respectively; difference 14.57 pg/ml 26% increase, 95%IC 1.90 to 27.23, P=0.02); however, with high interindividual variability. Similar results were found in the subgroup of patients with HHD and arginine vasopressin deficiency (AVP-D) (n=17), with HC showing a greater OXT increase at T90 (HC 68.95±4.37 vs. AVP-D 55.52±6.85 pg/ml; difference 13.30 pg/ml, 95%CI 0.95 to 25.65, P=0.03). HHD group had more depression and alexithymia symptoms, impaired sexual function and worse QoL in comparison with HC. The mean percentage change in OXT from T0 to T90 was negatively associated with depressive and alexithymia symptoms in HHD and anxiety in both groups.
Conclusion: The reduced OXT response to melatonin in HHD, supports the existence of an impaired OXT response in a subset of patients with HHD. The associations between OXT changes and psychopathology suggest its role in mood and QoL. These findings provide support for a clinically significant OXT-deficient state in HHD. Future studies could examine different doses of melatonin as a diagnostic tool to address OXT-D.
Volume 110
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